Cocaine usage is known to be a cause of myocardial infarction, but the exact mechanism by which it causes reduced blood flow is unknown. The pathophysiology behind this occurrence is thought to involve four different mechanisms: 1) increased myocardial oxygen demand secondary to increased catecholamine levels; 2) decreased myocardial perfusion secondary to coronary vasospasm; 3) cocaine-induced platelet activation and thrombogenesis; and 4) possibly direct myocardial cell damage by the cocaine itself. No human study has documented decreased cellular perfusion related to cocaine ingestion. After demonstrating in an earlier study that a 1.4 mg/kg dose of intranasal cocaine can be safely given, we are using a higher dose of intranasal cocaine, 2 mg/kg (up to a total 200 mg), to evaluate its effects on myocardial perfusion. We are detecting the decrease in myocardial blood flow by way of Positron Emission Tomography (PET) using an N-13 ammonia tracer. We are also evaluating the mechanism for this reduced perfusion by measuring mediators of coronary of coronary vasoconstriction and thrombosis (i.e. thromboxane, serotonin, endothelin, and nitric oxide), and determining if there are acute in vivo changes in endothelial function from cocaine ingestion with the aid of forearm plethrophysmography. We are also determining the effects of cocaine on electrocardiographic changes, in particular related to ventricular repolarization. Prolongation of ventricular repolarization by cocaine may be the mechanism that causes ventricular arrythmias and sudden death during cocaine intoxication.